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Updated: Jan 29, 2026
Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
Published on: March 21, 2021
miR-33 and RIP140 participate in LPS-induced acute lung injury
Background/Aim:
Pulmonary microvascular endothelial cells (PMVECs) play a pivotal role in the process of acute lung injury (ALI), which can be induced by lipopolysaccharide (LPS). Numerous reports have indicated that both miR-33 and RIP140 are involved in the inflammatory response in macrophages. In this study, we sought to investigate whether miR-33 and RIP140 participate in ALI induced by LPS.
Materials And Methods:
First, we isolated and identified PMVECs from BALB/c mice. Subsequently, both PMVECs and BALB/c mice were treated with PBS, LPS, or pyrrolidine dithiocarbamate (PDTC) plus LPS and divided into three groups: control (PBS), LPS (LPS), and L+P (LPS plus PDTC) groups. We assessed pathology by hematoxylin and eosin staining, and miR-33 and RIP140 expression levels were examined using quantitative PCR and Western blot analyses.
Results:
Our results demonstrated that LPS can induce PMVEC injury and ALI and that LPS treatment significantly decreased miR-33 expression compared with controls (P < 0.001, n = 5). On the contrary, RIP140 was markedly overexpressed by LPS treatment (P < 0.001, n = 5). However, this alteration can be inhibited by pretreatment with PDTC before LPS (P < 0.05, n = 5).
Conclusion:
This study is the first to confirm that both miR-33 and RIP140 participate in LPS-induced PMVEC injury and ALI, which may help uncover the mechanism of ALI
Insights
This study reveals that microRNA-33 (miR-33) and RIP140 are involved in lipopolysaccharide-induced acute lung injury (ALI) in pulmonary microvascular endothelial cells. Reduced miR-33 and increased RIP140 expression contribute to ALI pathogenesis.
Area of Science:
- Cell Biology
- Immunology
- Pulmonary Medicine
Background:
- Pulmonary microvascular endothelial cells (PMVECs) are critical in acute lung injury (ALI).
- Lipopolysaccharide (LPS) is a known inducer of ALI.
- Previous studies implicated miR-33 and RIP140 in macrophage inflammatory responses.
Purpose of the Study:
- To investigate the role of miR-33 and RIP140 in LPS-induced ALI.
- To determine if these molecules are involved in PMVEC injury during ALI.
Main Methods:
- Isolation and identification of PMVECs from BALB/c mice.
- Treatment of PMVECs and mice with PBS, LPS, or PDTC plus LPS.
- Assessment of lung pathology via hematoxylin and eosin staining.
- Quantification of miR-33 and RIP140 expression using qPCR and Western blot.
Main Results:
- LPS induced PMVEC injury and ALI.
- LPS significantly decreased miR-33 expression (P < 0.001).
- LPS significantly increased RIP140 expression (P < 0.001).
- PDTC pretreatment inhibited these alterations (P < 0.05).
Conclusions:
- This study provides the first evidence that miR-33 and RIP140 participate in LPS-induced PMVEC injury and ALI.
- These findings may elucidate the underlying mechanisms of ALI.
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